A 27-year-old man with an allergy to house dust mites was found to lack the Fc gammaRIIIb on his neutrophils. Cell surface marker and PCR techniques were used to investigate possible reasons for this deficiency. Agglutination and immunofluorescence assays using the man's neutrophils together with NA1- and NA2-specific antibodies were negative, and there was no reaction with the Fc gammaRIII-specific mAb 3G8. Indirect immunofluorescence demonstrated the presence of the CD24 molecule, which, like the Fc gammaRIIIb, is anchored to the cell membrane by glycosylphosphatidylinositol. Thus a lack of the Fc gammaRIIIb cell membrane anchor was excluded. PCR analysis confirmed the absence of the NA1 and NA2 alleles. The individual was therefore typed as NA"null". The products of those genes located together with the Fc gammaRIIIB gene within a complex on chromosome 1 (q23-24) were examined. Fc gammaRII was demonstrated on monocytes and B cells with the use of Fc gammaRII-specific monoclonal antibodies. About 5% of the individual's peripheral blood monocytes were positive with the 3G8 antibody, indicating the presence of Fc gammaRIIIa. From these data we concluded that the Fc gammaRIIIb deficiency on the neutrophil cell surface of this individual is due to a lack of the Fc gammaRIIIB gene while excluding a lack of the Fc gammaRIIA and the Fc gammaRIIIA genes.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1007/s002770050392 | DOI Listing |
J Biol Chem
February 2011
Centre de Recherche du Centre Hospitalier Universitaire de Québec, Department of Microbiology-Infectiology and Immunology, Faculty of Medicine, Laval University, Québec City, Québec G1V 4G2, Canada.
Human neutrophils constitutively express a unique combination of FcγRs, namely FcγRIIa and FcγRIIIb. Numerous lines of evidence support the concept that these FcγRs generate only partially characterized intracellular signals. However, despite the fact that both receptors are likely to be engaged simultaneously in a physiological setting, no recent publications have investigated the distinct, although partially convergent, results of their joint activation in IgG-dependent responses.
View Article and Find Full Text PDFImmunology
July 2005
The Multiple Sclerosis National Competence Centre, Haukeland University Hospital, University of Bergen, N-5021 Bergen, Norway.
Receptors for the Fc domain of IgG (Fc gammaR) play a critical role in linking cellular and humoral immunity. The various Fc gammaR genotypes may contribute to differences in infectious and immune-related diseases in various ethnic populations. The Samis are the aboriginal inhabitants of Norway and Fennoscandinavia and differ ethnically from the Norwegians.
View Article and Find Full Text PDFJ Neuroimmunol
May 2005
Department of Neurology G03.228, University Medical Center Utrecht, Heidelberglaan 100, 3584 CX Utrecht, The Netherlands.
Macrophages and ganglioside-specific IgG are involved in the pathogenesis of Guillain-Barre syndrome (GBS). Leukocyte IgG receptors (Fc gammaR) confer potent cellular effector functions to the specificity of IgG. The efficacy of IgG-mediated cellular inflammatory responses is determined by functional polymorphisms of three Fc gammaR subclasses (Fc gammaRIIa: H131/R131; Fc gammaRIIIa: V158/F158; Fc gammaRIIIb: NA1/NA2).
View Article and Find Full Text PDFJ Periodontol
May 2002
Dental Research Center, University of Medicine and Dentistry of New Jersey, Newark, USA.
Background: Receptors for the Fc fragment of immunoglobulin G (Fc gammaRs) play a crucial role in host defense against bacterial infection by linking humoral and cell-mediated immune responses. Allelic variants of certain Fc gammaRs have been shown to differ relative to their biologic activity. Thus, genes encoding allotypes with diminished activity have been suggested as potential risk factors for infectious diseases.
View Article and Find Full Text PDFArthritis Rheum
October 1998
Central Laboratory of The Netherlands Red Cross Blood Transfusion Service, and Academic Medical Center, University of Amsterdam.
Objective: To study whether the Fc gammaRIIIA-158V/F polymorphism, which affects IgG binding affinity, is a risk factor for systemic lupus erythematosus (SLE).
Methods: We genotyped a group of 70 Caucasian SLE patients for all known Fc gammaR polymorphisms. Of this group, 45 patients (64%) had nephritis.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!